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dc.contributor.authorYoung, D F
dc.contributor.authorGaliano, M
dc.contributor.authorLemon, K
dc.contributor.authorChen, Y-H
dc.contributor.authorAndrejeva, Jelena
dc.contributor.authorDuprex, P
dc.contributor.authorRima, B K
dc.contributor.authorRandall, Richard Edward
dc.date.accessioned2010-12-21T10:06:03Z
dc.date.available2010-12-21T10:06:03Z
dc.date.issued2009-11
dc.identifier.citationYoung , D F , Galiano , M , Lemon , K , Chen , Y-H , Andrejeva , J , Duprex , P , Rima , B K & Randall , R E 2009 , ' Mumps virus Enders strain is sensitive to interferon (IFN) despite encoding a functional IFN antagonist ' Journal of General Virology , vol. 90 , no. 11 , pp. 2731-2738 . https://doi.org/10.1099/vir.0.013722-0en
dc.identifier.issn0022-1317
dc.identifier.otherPURE: 455045
dc.identifier.otherPURE UUID: b5364ad2-ee97-49a7-9488-961ef5da3248
dc.identifier.otherWOS: 000271440500019
dc.identifier.otherScopus: 70350443463
dc.identifier.otherORCID: /0000-0002-9304-6678/work/60426972
dc.identifier.urihttp://hdl.handle.net/10023/1640
dc.description.abstractAlthough the Enders strain of mumps virus (MuV) encodes a functional V protein that acts as an interferon (IFN) antagonist, in multi-cycle growth assays MuV Enders grew poorly in naive ('IFN-competent' Hep2) cells but grew to high titres in 'IFN-compromised' Hep2 cells. Even so, the growth rate of MuV Enders was significantly slower in 'IFN-compromised' Hep2 cells when compared with its replication rate in Vero cells and with the replication rate of parainfluenza virus type 5 (a closely related paramyxovirus) in both naive and 'IFN-compromised' Hep2 cells. This suggests that a consequence of slower growth is that the IFN system of naive Hep2 cells can respond quickly enough to control the growth of MuV Enders. This is supported by the finding that rapidly growing variants of MuV Enders that were selected on 'IFN-compromised' Hep2 cells (i.e. in the absence of any selection pressure exerted by the IFN response) also grew to high titres on naive Hep2 cells. Sequencing of the complete genome of one of these variants identified a single point mutation that resulted in a substitution of a conserved asparagine by histidine at position 498 of the haemagglutinin-neuraminidase protein, although this mutation was not present in all rapidly growing variants. These results support the concept that there is a race between the ability of a cell to detect and respond to virus infection and the ability of a virus to block the IFN response. Importantly, this emphasizes that factors other than viral IFN antagonists influence the sensitivity of viruses to IFN.
dc.format.extent8
dc.language.isoeng
dc.relation.ispartofJournal of General Virologyen
dc.rights(c)2009 SGM. Article available under publisher's Open Optionen
dc.subjectDependent rna-polymeraseen
dc.subjectV-proteinen
dc.subjectAntiviral responsesen
dc.subjectRIG-Ien
dc.subjectParainfluenza virus-5en
dc.subjectGene-expressionen
dc.subjectDegredationen
dc.subjectInductionen
dc.subjectCellsen
dc.subjectTransductionen
dc.subjectQR355 Virologyen
dc.subject.lccQR355en
dc.titleMumps virus Enders strain is sensitive to interferon (IFN) despite encoding a functional IFN antagonisten
dc.typeJournal articleen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews.School of Biologyen
dc.contributor.institutionUniversity of St Andrews.Biomedical Sciences Research Complexen
dc.identifier.doihttps://doi.org/10.1099/vir.0.013722-0
dc.description.statusPeer revieweden
dc.identifier.urlhttp://www.scopus.com/inward/record.url?scp=70350443463&partnerID=8YFLogxKen


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